Ulcerative colitis (UC) is a chronic inflammatory disorder of the mucosa and submucosa of the colon. Although the pathogenesis of UC is multifactorial and idiopathic, a growing body of evidence suggests that proinflammatory mediators produce excess reactive oxygen species (ROS) which can cause oxidative damage resulting in oxidative stress in UC patients. Proof-of-concept preclinical studies using knockout mouse models conducted by Cureveda's founders and others have demonstrated that the selective activation of transcription factor signaling is a potential strategy for the treatment of oxidative-stress-related inflammatory diseases. The transcription factor Nrf2 has emerged as a central player in regulating antioxidant defenses and innate immune response. In addition, our preliminary evidence suggests that augmenting Nrf2 inhibits Th-17 driven inflammation. Cureveda's founders have identified a potent small molecule activator of Nrf2 signaling, VEDA-1209, which has potential as a therapeutic for UC. We hypothesize that, by reducing the rates of oxidative reactions and increasing the rates of antioxidative reactions, VEDA-1209 reduces inflammation-related injury. The proposed Phase I project aims to evaluate VEDA-1209 for the treatment of ulcerative and pharmacodynamic studies and determining its therapeutic efficacy by evaluating markers of oxidative stress, inflammation and tissue injury in the mouse model. Positive outcomes will support further preclinical development of VEDA-1209 in phase II SBIR.